The present invention relates generally to implantable medical interventional devices which provide a range of pacing, cardioversion, and defibrillating functions to preserve the life and stamina of the patient, and more particularly to an implantable defibrillator that exhibits improved hemodynamic response and enhanced myocardial stability to vastly improve the quality of life of the patient. As used herein, the terminology "implantable defibrillator" is intended to refer broadly to a device which is adapted to perform a variety of essential cardiac interventional functions, as is typically the case in actual medical device practice, and not merely limited to defibrillation therapy.
Administering therapy from implantable defibrillators has proven to be highly effective in preventing sudden cardiac death. Nonetheless, many patients provided with defibrillators suffer from myocardial failure attributable to serious underlying disease that contributes to electrical instability and reduced myocardial function. The determinants of cardiac output (the volume of blood discharged from the ventricle per minute), especially during exercise, are volume (the volume of blood discharged from the ventricle with each contraction) and heart rate (cardiac output=stroke volume.times.heart rate). While the normal heart is capable of increasing its stroke volume by a factor of 50% when the patient goes from conditions of rest to exercise, the majority of patients who are candidates for an implantable defibrillator lack that degree of contractile reserve. For such patients it is essential that the implanted device adapt the heart rate to closely if not precisely match the limited cardiac output to the needs of the patient's body.
While a healthy person or a patient who may be only slightly myocardially compromised has mechanisms that enable his or her cardiac output to adapt to a wider variation of stroke volume, the typical defibrillator patient lacks any such mechanism by which to adapt, and instead predominantly adjusts cardiac output by means of a modification of heart rate. But if the patient's heart rate is too low for a given exercise load, an increase in endiastolic left ventricular filling pressure is experienced. In essence, the heart is simply incapable on its own of pumping sufficient blood into systemic circulation, which results in congestion of the pulmonary system and reduced oxygen pressure, and also affects the stability of the myocardium. Increased endiastolic pressures cause an increased stress to the myocardial wall which is a factor in the triggering of ventricular extrasystoly (i.e., premature ventricular contraction or PVC). Although the malady is commonly experienced in otherwise relatively healthy adults who engage in heavy smoking or experience severe emotional excitement, it is most of ten encountered to be of multifocal origin in cases of organic heart disease or digitalis intoxication, and can lead to ventricular tachycardia, and ultimately, ventricular fibrillation.
In the past, a wide variety of sensors has been proposed for potential control of ventricular rate. But not all of the potential sensor signals are suitable for heart rate control in patients needing an implantable defibrillator. Control that produces a heart rate which is either too slow or too fast in terms of the patient's metabolism, is inappropriate. A sensor that produces these types of improper responses, for example because of its sensitivity to environmental noise sources or to other phenomena which are not matched to the body metabolism, is unsuitable for use in implantable defibrillators or other cardiac interventional devices.
It is therefore a principal aim of the present invention to provide an implantable defibrillator with improved hemodynamic response, and which provides greater myocardial stability. The desire is to achieve these results by use in the medical interventional device of a particularly suitable and effective rate control signal, so that the frequency of device intervention by delivery of either cardioverting or defibrillating shocks will be substantially reduced. Ultimately, although the device is intentionally implemented to deliver such therapy repeatedly despite its battery-operated nature, a marked reduction in the number of times the patient will receive shocks from the device by virtue of a more circumspect hemodynamic response of the device will substantially lessen duress on the patient's myocardial function and other aspects of his physiology, including orthopedic distress, for example, and with it, considerably less pain and general discomfort to the patient. Furthermore, reducing the number of shocks that must be generated by the device is effective to conserve energy and will thereby prolong the useful life of the device. A more appropriate rate control can also serve to increase the patient's capacity for exercise, and with it, improve the patient's quality of life.